NDLI: CoCl$_{2}$ induces apoptosis through the mitochondria- and death receptor-mediated pathway in the mouse embryonic stem cells

Content Provider	Springer Nature Link
Author	Lee, Jin Ha Choi, Seong Ho Baek, Min Woo Kim, Mi Hwa Kim, Heong Jun Kim, Sun Hun Oh, Sang Jin Park, Hong Ju Kim, Won Jae Jung, Ji Yeon
Copyright Year	2013
Abstract	Embryonic hypoxia/ischemia is a major cause of a poor fetal outcome and future neonatal and adult handicaps. However, biochemical cellular events in mouse embryonic stem (mES) cells during hypoxia remains unclear. This study investigated the underlying mechanism of apoptosis in mES cells under CoCl$_{2}$-induced hypoxic/ischemic conditions. CoCl$_{2}$ enhanced the expression of hypoxia-inducible factor-1α (HIF-1α) and the accumulation of reactive oxygen species in mES cells. The CoCl$_{2}$-treated mES cells showed a decrease in cell viability as well as typical apoptotic changes, cell shrinkage, chromatin condensation, and nuclear fragmentation and an extended G$_{2}$/M phase of the cell cycle. CoCl$_{2}$ augmented the release of cytochrome c into the cytosol from the mitochondria with a concomitant loss of the mitochondrial transmembrane potential (ΔΨ$_{m}$) and upregulated the voltage-dependent anion channel. In addition, CoCl$_{2}$-induced caspase-3, -8, and -9 activation and upregulation of p53 level, whereas downregulated Bcl-2 and Bcl-xL, a member of the anti-apoptotic Bcl-2 family in mES cells. Furthermore, CoCl$_{2}$ led to the upregulation of Fas and Fas-ligand, which are the death receptor assemblies, as well as the cleavage of Bid in mES cells. These results suggest that CoCl$_{2}$ induces apoptosis through both mitochondria- and death receptor-mediated pathways that are regulated by the Bcl-2 family in mES cells.
Starting Page	133
Ending Page	140
Page Count	8
File Format	PDF
ISSN	03008177
Journal	Molecular and Cellular Biochemistry
Volume Number	379
Issue Number	1-2
e-ISSN	15734919
Language	English
Publisher	Springer US
Publisher Date	2013-04-09
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	CoCl$_{2}$ mES cells Apoptosis Bcl-2 family Caspase Fas Fas-L Biochemistry Medical Biochemistry Oncology Cardiology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Medicine Clinical Biochemistry Molecular Biology

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